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Biography

My prior studies focused on the pathogenesis of
cigarette-smoke (CS) -induced lung diseases such as chronic obstructive
pulmonary disease (COPD), wherein we demonstrated that the
IL-18 system plays an important role in the pathogenesis of CS-induced
emphysematous lung destruction. These studies led me to question the effect of CS
on innate immunity on the interaction between the host and microorganisms and,
for this purpose, I had established a murine cigarette smoke and virus
co-exposure model. These studies revealed important insight into the
interaction between CS and the innate immunity resulting in a publication in
the Journal of Clinical Investigation.
In that study, we identified that CS smoke selectively augments respiratory
antiviral innate immune responses via a MAVS-RLHs antiviral signaling pathway. To
gain better understanding of the mechanisms, my laboratory is focusing on the
role(s) of mitochondrial dysfunction and immune dysregulation in the setting of
smoking exposure. By applying recent state-of-art knowledge of mitochondrial
biology, our research goal is to establish mitochondrial dysfunction and
mitochondrial injury/damage responses as a key event in the pathogenesis of
COPD and CS-and virus-associated disorders and as such, to provide a new
perspective of our understanding of COPD and CS-and virus-associated disorders.

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